Richardson P D, Withrington P G
Circ Res. 1978 Oct;43(4):496-503. doi: 10.1161/01.res.43.4.496.
The hepatic arterial and hepatic portal venous vascular beds of the chloralose-urethane anesthetized dog were perfused simultaneously in situ. Vasopressin (10 mU = 1 unit) was injected in graded increasing doses into the hepatic artery and into the portal vein. Both intra-arterial and intraportal vasopressin elicited both hepatic arterial vasoconstriction and hepatic venous dilation; the delay in onset of both hepatic vascular effects was significantly shorter than that for any succeeding systemic effects (a rise in systemic arterial pressure and fall in heart rate), showing that they were not attributable to recirculation or to arterial baroreceptor reflexes. Injections of vasopressin into the inferior vena cava at the level of the hepatic veins consistently produced smaller hepatic vascular effects than either intra-arterial or intraportal injections of the same doses. The results are discussed in the context of the therapeutic role of vasopressin in controlling gastrointestinal bleeding and portal hypertension.
对用氯醛糖-乌拉坦麻醉的狗的肝动脉和肝门静脉血管床进行原位同步灌注。将血管加压素(10 mU = 1单位)以递增剂量分别注入肝动脉和门静脉。动脉内和门静脉内注射血管加压素均引起肝动脉血管收缩和肝静脉扩张;这两种肝血管效应的起效延迟明显短于任何后续的全身效应(全身动脉压升高和心率下降),表明它们并非归因于再循环或动脉压力感受器反射。在肝静脉水平向下腔静脉注射血管加压素,与相同剂量的动脉内或门静脉内注射相比,始终产生较小的肝血管效应。本文结合血管加压素在控制胃肠道出血和门静脉高压方面的治疗作用对结果进行了讨论。